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Principles of Disease > Hypersensitivity and Autoimmunity > Flashcards

Hypersensitivity and Autoimmunity Flashcards

1
Q

What is autoimmune disease?

A

An autoimmune disease is a disease which involves a failure/breakdown in the part of the immune system which maintains tolerance to self-tissues.

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2
Q

Who can develop autoimmune disease?

A

Anyone.

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3
Q

What characterises autoimmune disease in terms of mortality and morbidity?

A

Low mortality but very high morbidity.

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4
Q

Is there a cure for autoimmune disease?

A

No- therapies are managed on a symptomatic basis rather than a cure basis.

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5
Q

What is the loss of tolerance in autoimmune disease usually caused by?

A

Abnormal selection or lack of control of self-reactive lymphocytes.

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6
Q

What are hypersensitivity responses?

A

Hypersensitivity responses are hyper (too much) responses from the immune system- they may produce tissue injury and cause serious disease.

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7
Q

What are the 4 categories of hypersensitivity response?

A

I, II , III , IV

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8
Q

What types of hypersensitivity response are antibody-mediated?

A

I , II , III

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9
Q

What types of hypersensitivity response are T-cell mediated?

A

IV

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10
Q

What types of hypersensitivity responses do autoimmune diseases usually tend to fall into?

A

II , III , IV

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11
Q

What do Type I hypersensitivity reactions involve?

A

Allergy

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12
Q

What happens during Type I hypersensitivity reactions?

A

Initiated by allergen, stimulating TH2 reactions and IgE production. IgE binds to a FceR1 protein and sensitises mast cells to produce an immune response.

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13
Q

What do Type I reactions stimulate?

A

TH2 reactions and IgE binding to FceR1 proteins to sensitise mast cells.

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14
Q

What protein does IgE bind to in order to sensitise mast cells?

A

FceR1.

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15
Q

What are the effects of mast cell stimulation?

A

Vasodilation, bronchioconstriction, oedema, vascular congestion.

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16
Q

What is seen in the immediate hypersensitivity reaction to allergy?

A

IgE mediation of mast cells to produce vasodilation/oedema/vascular congestion.

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17
Q

What is seen in the late-phase hypersensitivity reaction to allergy?

A

Inflammatory infiltrate rich in eosinophils, neutrophils, and T-cells.

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18
Q

When does an immediate hypersensitivity reaction occur?

A

Within minutes of allergen exposure.

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19
Q

When does a late-phase hypersensitivity reaction occur?

A

Within 2-24 hours of allergen exposure.

20
Q

What is atopy?

A

Predisposition to allergy- patients more susceptible to autoimmune conditions such as asthma/eczema/thyroiditis.

21
Q

What is higher in atopic patients?

A

IgE levels.

22
Q

What do Type II hypersensitivity reactions involve?

A

Cytotoxic cells.

23
Q

What happens in Type II hypersensitivity reactions?

A

Mediated by IgG/IgM antibodies binding to cell-surface antigens or matrix-associated antigens on basement membrane. This results in complement leading to the inflammatory response or involvement with cytotoxic T-cells.

24
Q

What are Type II hypersensitivity reactions mediated by?

A

IgG/IgM antibodies binding to cell/matrix antigens.

25
Q

What does mediation result in within Type II hypersensitivity reactions?

A

Complement- inflammatory response

Cytotoxic cell involvement.

26
Q

Can Type II reactions include autoimmune disease?

A

Yes- if the antigen involved is a self-antigen.

27
Q

What do Type III hypersensitivity reactions involve?

A

Formation of immune complexes.

28
Q

What happens in Type III hypersensitivity reactions?

A

Soluble antigens bind with IgG in a ration that results in the accumulation of immune complexes (aggregates of antibody/antigen). These form on vascular epithelial cells and are not phagocytose so lead to a cascade of inflammatory events. (Mast cells, Complement, Permeability).

29
Q

What are immune complexes?

A

Aggregates of antibody/antigen.

30
Q

Where do immune complexes form?

A

Vascular epithelium of blood vessels.

31
Q

Can immune complexes be phagocytosed?

A

No.

32
Q

What happens during the cascade of inflammatory events caused by immune complexes?

A

IgG stimulates mast cells
Complement activation- pro inflammatory C3a/C5a
Increased vascular permeability due to chemotactic recruitment of neutrophils and macrophages.

33
Q

What is recruited in the complement activation in this inflammatory cascade?

A

C3a / C5a

34
Q

Why is there an increased vascular permeability within the inflammatory cascade?

A

Chemotactic recruitment of neutrophils and macrophages.

35
Q

How are immune complexes removed?

A

Lysosomal degradation- results in damage to local cells resulting in coagulation pathway activation.

36
Q

Why is the coagulation pathway activated during Type III reactions?

A

Localised cell damage due to the lysosomal degradation of immune complexes.

37
Q

What do Type IV hypersensitivity reactions involve?

A

T-cells.

38
Q

Are Type IV reactions antigen-mediated?

A

No- regulated by T-cells and involve effector cells.

39
Q

What happens during Type IV hypersensitivity reactions?

A

Involve tissue damage mediated by activated macrophages and cytotoxic T-cells.

40
Q

What are the 3 types of Type IV reaction?

A

CD4 Th1- delayed
CD4 Th2- inhalation
CD8 cytotoxic T lymphocyte- transplant rejection

41
Q

What happens during CD4 Th1 reactions?

A

Delayed reaction.

42
Q

What happens during TD4 Th2 reactions?

A

Soluble antigen is inhaled- eosinophil recruitment and activation occurs with cytokine and inflammatory mediator release. Cause of asthma / rhinitis.

43
Q

What happens during CD8 cytotoxic T-lymphocyte reactions?

A

Cell killing and tissue injury- seen within tissue transplant rejection.

44
Q

What is immunological tolerance?

A

Immunological tolerance is a state of tolerance in the immune system when it would usually be expected to excite an immunological response.

45
Q

What is the difference between systemic autoimmune disease and tissue-specific autoimmune disease?

A

Systemic autoimmune disease involves the holistic system whereas tissue-specific autoimmune disease is localised.

Principles of Disease (22 decks)

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